scholarly journals 2021 Korean Diabetes Association Clinical Practice Guidelines for Diabetes: Diabetic Kidney Disease

2021 ◽  
Vol 22 (4) ◽  
pp. 268-273
Author(s):  
Nam Hoon Kim

Diabetic kidney disease is one of the most serious complications of type 2 diabetes and a leading cause of end-stage kidney disease. Recently, the Korean Diabetes Association released a new version of clinical practice guidelines including substantial changes in the management of diabetic kidney disease. Of note, sodium-glucose cotransporter 2 inhibitors and glucagon-like peptide-1 receptor agonists are now the preferred glucose-lowering agents for reduced glomerular filtration rate or albuminuria. Convincing evidence from cardiovascular or renal outcome trials supports the recommendation of those drugs. This review summarizes the results of recent clinical studies on diabetic kidney disease and explains new clinical recommendations based on them.

2018 ◽  
Vol 315 (6) ◽  
pp. F1519-F1525 ◽  
Author(s):  
Brad P. Dieter ◽  
Radica Z. Alicic ◽  
Katherine R. Tuttle

Diabetic kidney disease (DKD), one of the most common and severe microvascular complications of diabetes, is the leading cause of chronic kidney disease and end-stage kidney disease worldwide. Since the development of renin-angiotensin system inhibition nearly three decades ago, no new therapeutic agents have received regulatory approval for treatment of DKD. Glucagon-like peptide-1 (GLP-1) receptor agonists, a class of newer antihyperglycemic agents, have shown promise for prevention of DKD onset and progression. This perspective summarizes clinical and experimental observations to give insight into biological mechanisms beyond glycemic control, such as natriuresis and anti-inflammatory actions, for preservation of kidney function in patients with diabetes.


2022 ◽  
Vol 11 (2) ◽  
pp. 378
Author(s):  
Hanny Sawaf ◽  
George Thomas ◽  
Jonathan J. Taliercio ◽  
Georges Nakhoul ◽  
Tushar J. Vachharajani ◽  
...  

Diabetic kidney disease (DKD) is the most common cause of end-stage kidney disease (ESKD) in the United States. Risk factor modification, such as tight control of blood glucose, management of hypertension and hyperlipidemia, and the use of renin–angiotensin–aldosterone system (RAAS) blockade have been proven to help delay the progression of DKD. In recent years, new therapeutics including sodium-glucose transport protein 2 (SGLT2) inhibitors, endothelin antagonists, glucagon like peptide-1 (GLP-1) agonists, and mineralocorticoid receptor antagonists (MRA), have provided additional treatment options for patients with DKD. This review discusses the various treatment options available to treat patients with diabetic kidney disease.


Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 789
Author(s):  
Agata Winiarska ◽  
Iwona Filipska ◽  
Monika Knysak ◽  
Tomasz Stompór

Phosphorus is an essential nutrient that is critically important in the control of cell and tissue function and body homeostasis. Phosphorus excess may result in severe adverse medical consequences. The most apparent is an impact on cardiovascular (CV) disease, mainly through the ability of phosphate to change the phenotype of vascular smooth muscle cells and its contribution to pathologic vascular, valvular and other soft tissue calcification. Chronic kidney disease (CKD) is the most prevalent chronic disease manifesting with the persistent derangement of phosphate homeostasis. Diabetes and resulting diabetic kidney disease (DKD) remain the leading causes of CKD and end-stage kidney disease (ESRD) worldwide. Mineral and bone disorders of CKD (CKD-MBD), profound derangement of mineral metabolism, develop in the course of the disease and adversely impact on bone health and the CV system. In this review we aimed to discuss the data concerning CKD-MBD in patients with diabetes and to analyze the possible link between hyperphosphatemia, certain biomarkers of CKD-MBD and high dietary phosphate intake on prognosis in patients with diabetes and DKD. We also attempted to clarify if hyperphosphatemia and high phosphorus intake may impact the onset and progression of DKD. Careful analysis of the available literature brings us to the conclusion that, as for today, no clear recommendations based on the firm clinical data can be provided in terms of phosphorus intake aiming to prevent the incidence or progression of diabetic kidney disease.


Diabetology ◽  
2021 ◽  
Vol 2 (1) ◽  
pp. 31-35
Author(s):  
Keiichiro Matoba

Diabetic kidney disease (DKD) is a global epidemic leading to end-stage renal disease (ESRD) and susceptibility to cardiovascular disease, with few therapeutic interventions. A hallmark of DKD is the activation of the renin-angiotensin-aldosterone system and hemodynamic changes in glomerulus. Although intensive therapy with agents that targets those abnormalities lowers the risk of DKD progression, it does not completely abolish the risk of ESRD and cardiovascular events. Recent studies have illustrated the importance of renal inflammation, oxidative stress, and activated Rho-associated protein kinase (ROCK) signaling as essential pathogenesis for the development of DKD. In this commentary, these topics will be discussed.


2003 ◽  
Vol 284 (6) ◽  
pp. F1138-F1144 ◽  
Author(s):  
Kumar Sharma ◽  
Peter McCue ◽  
Stephen R. Dunn

Diabetic nephropathy is increasing in incidence and is now the number one cause of end-stage renal disease in the industrialized world. To gain insight into the genetic susceptibility and pathophysiology of diabetic nephropathy, an appropriate mouse model of diabetic nephropathy would be critical. A large number of mouse models of diabetes have been identified and their kidney disease characterized to various degrees. Perhaps the best characterized and most intensively investigated model is the db/ db mouse. Because this model appears to exhibit the most consistent and robust increase in albuminuria and mesangial matrix expansion, it has been used as a model of progressive diabetic renal disease. In this review, we present the findings from various studies on the renal pathology of the db/ db mouse model of diabetes in the context of human diabetic nephropathy. Furthermore, we discuss shortfalls of assessing functional renal disease in mouse models of diabetic kidney disease.


2016 ◽  
Vol 20 (4) ◽  
pp. 510-510
Author(s):  
Shigeo Horie ◽  
Toshio Mochizuki ◽  
Satoru Muto ◽  
Kazushige Hanaoka ◽  
Yoshimitsu Fukushima ◽  
...  

2020 ◽  
pp. 68-77
Author(s):  
Samuel N Uwaezuoke ◽  
Adaeze C Ayuk

Diabetic kidney disease (DKD) is defined as a clinical syndrome consisting of persistent macroalbuminuria, progressive decline in glomerular filtration rate (GFR), hypertension, increased cardiovascular disease events, and the associated mortality of these conditions. The disease evolves from the microvascular complications of poorly controlled Type 1 diabetes mellitus (T1DM) and Type 2 diabetes mellitus (T2DM). The pathogenic pathways comprise renal haemodynamic changes, ischaemia and inflammation, and overactive renin–angiotensin–aldosterone system (RAAS), through which several events cascade down from hyperglycaemia to renal fibrosis. Conventional and novel renoprotective strategies target modifiable DKD risk factors and specific stages of the pathogenic pathways, respectively. Although these strategies may slow DKD progression to end-stage kidney disease (ESKD), novel drugs are still undergoing trials for validation in human participants. This narrative review appraises these renoprotective strategies and highlights the current clinical staging and pathogenesis of the disease.


Author(s):  
Salbiah Binti Isa ◽  
Rohayu Hami ◽  
Alma’ Norliana JA ◽  
Siti Salmah Noordin ◽  
Tuan Salwani Tuan Ismail

Diabetic kidney disease (DKD) is a known complication of diabetes mellitus that increases patients’ risks of developing end-stage renal failure requiring dialysis treatment and vulnerability of fatal outcomes resulted from cardiovascular events. Therefore, a good diabetic control among patients with DKD is essential. Nevertheless, monitoring glycaemia in DKD is very challenging. The use of the gold standard glycaemic marker, haemoglobin A1c (HbA1c), is complicated by many hindrances associated with both biochemical and physiological derangements of DKD. Despite the constraints, the Kidney Disease Improving Global Outcome has recommended the use of HbA1c as a reliable glycaemic marker in DKD patients, whose estimated glomerular filtration rate is down to 30 millilitres/minute per 1.73 meter2 . In this article, we discuss the reliability and limitations of HbA1c as an advocated glycaemic marker in DKD. Considering that the reliability of HbA1c is highly dependent on the interpretation of the results, we also highlighted the common potential factors that can affect HbA1c interpretation in patients with DKD. The article also discusses the issues related to the utility of glycated albumin and serum fructosamine as alternative glycaemic biomarkers, and continuous glucose monitoring as a complementary marker to HbA1c in clinical practice. Understanding the HbA1c values and their limitations is important to ensure accurate interpretation of glycaemic status and to achieve optimal diabetic control in patients with DKD.


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